| Backgroud:Ischemia reperfusion injury is an important pathophysio logic phenomenon during the perioperative time, especially for some emergency time. Restoring its perfusion and oxygenation timely is an effective manner for treating and rescuing, However, after the reperfusion, the injury is more serious, more durable, directly endangered the whole body. Ischemia reperfusion injury is an inflammation in essence, Inflammation is a physiological function of the body repairing necrotic tissue, maintaining defense. What is more, the excessive inflammatory reaction will lead to the important organs damage. Ischemic preconditioning and ischemic postconditioning has confirmed has the effect of reducing ischemia reperfusion injury through the PTEN/PI-3K/Akt/GSK-3? signaling pathway. Myocardial infarction, as a high incidence and high fatality rate, is a main complications of clinical, which can lead remote organ to ischemia reperfusion injury by chemical neurotransmitter. Whatever, lung is the most vulnerable organ in the body, when excessive inflammation exploded, which can leads to regulation mechanism disorder. Therefore the signal pathway of acute lung injury induced by myocardial ischemia reperfusion, the inflammation factor of acute lung injury induced by myocardial ischemia reperfusion and the protective effects of ischemic postconditioning is a hotly highlights in scientific research.Part One:To observe acute lung injury induced by myocardial ischemia reperfusion and the protective effect of ischemic postconditioningObjective:To investigate the effect of acute lung injury induced by myocardial ischemia reperfusion and the function of ischemic postconditioning.Methods:30SD rats were allocated into3groups, group sham (group S), group myocardial ischemia reperfusion (group I/R), group ischemic postconditioning (group IPost). Myocardial ischemia reperfusion was induced by occlusion of anterior descending branch of left coronary artery for30min followed by120min reperfusion. Ischemic postconditioning received3cycles of10s reperfusion followed by10s ischemia at the end of30min myocardial ischemia. The lung was immediately removed for determination of histopathology, apoptosis factor, TUNEL.Results:Group I/R significantly increased the number of apoptotic neuronal, down-regulated Bcl-2expression and up-regulated Bax, Caspase-3expression as compared with group S (P<0.01).Conclusions:Myocardial ischemia reperfusion can lead to acute lung injury, ischemic postconditioning has a protective effect on acute lung injury induced by myocardial ischemia reperfusion. Part Two:The effect of PI-3K/Akt signaling pathway on acute lung injury induced by myocardial ischemia reperfusion and ischemic postconditioningObjective:To investigate the effect of PI-3K/Akt signaling pathway on acute lung injury induced by myocardial ischemia reperfusion and ischemic postconditioning.Methods:40SD rats were allocated into4groups, group sham (group S), group myocardial ischemia reperfusion (group I/R), group ischemic postconditioning (group IPost), group ischemic postconditioning+PTEN inhibitor (group IPost?). Inhibitor Bpv1mg/kg was given before operation. Myocardial ischemia reperfusion was induced by occlusion of anterior descending branch of left coronary artery for30min followed by120min reperfusion. Ischemic postconditioning received3cycles of10s reperfusion followed by10s ischemia at the end of30min myocardial ischemia. The lung was immediately removed for determination of histopathology, apoptosis factor, TUNEL and western blotting.Results:Group I/R significantly increased the number of apoptotic neuronal, down-regulated Bcl-2expression and up-regulated Bax, Caspase-3expression as compared with group S (P<0.01). p-GSK-3? was down-regulated in group I/R compared with other three groups (P<0.05). There were no significant different between group IPost and IPostI (P>0.05).Conclusions:The inhibitor Bpv doesn't develop the function as preconceived in acute lung injury induced by myocardial ischemia reperfusion. Part Three:The effect of inflammatory factor on acute lung injury induced by myocardial ischemia reperfusion and ischemic postconditioningObjective:To investigate the effect of inflammatory factor on acute lung injury induced by myocardial ischemia reperfusion and ischemic postconditioning.Methods:Male Sprague-Dawley (SD) rats were randomly assigned into four groups: sham (S) group, myocardial ischemia/reperfusion (IR) group, ischemic post-conditioning (IPost) group and ischemic post-conditioning+GSK-3? inhibitor (IPostI) group. Myocardial I/R was induced by occlusion of anterior descending branch of left coronary artery for30min followed by120min reperfusion. Post-conditioning was received3cycles of10s reperfusion followed by10s ischemia at the end of30min myocardial ischemia. GSK-3? inhibitor was peritoneal injected10min before the operation. The lung injury was assessed by the histopathology changes. The expression of Bax, Bcl-2, IL-6, IL-8and IL-10were measured with immunohistochemistry. Cell Apoptosis was measured by TUNEL. The expression of GSK-3? and caspase-3were determined by western blotting.Results:During the period of myocardial ischemia/reperfusion, the structures of lung was damaged seriously, and the interstitial capillaries were filled with leucocytosis. The expression of Bax, IL-6, IL-8, TUNEL and cleaved caspase-3in the lung were significantly increased, and the expression of Bcl-2, IL-10and p-GSK-3? were decreased in the group of myocardial ischemia/reperfusion. Ischemic post-conditioning effectively reversed these changes in protein expression following IR.Conclusion:It might be concluded that inflammatory factor can lead to acute lung injury by immediate activating GSK-3p. Post-conditioning can partly attenuate myocardial I/R-induced lung injury. |
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